Stark G, Sterz F, Stark U, Bachernegg M, Decrinis M, Lueger A, Pilger E, Tritthart H A
Department of Internal Medicine, Karl-Franzens-University, Graz, Austria.
Basic Res Cardiol. 1993 Jan-Feb;88(1):23-32. doi: 10.1007/BF00788527.
Negative chronotropic and dromotropic effects of adenosine seem to be responsible for its antiarrhythmic action on supraventricular tachyarrhythmias. To further characterize the effects of adenosine on supraventricular arrhythmias heart rate, conduction, refractoriness, the time to steady-state of AV-nodal conduction slowing and of sinus rate reduction were evaluated. Changes of heart rate, conduction intervals and effective refractory periods were determined by the use of a high-resolution ECG recording technique in isolated guinea pig hearts perfused by the method of Langendorff. Adenosine in concentrations of 3 and 10 microM reduced sinus rate and prolonged AV-nodal conduction significantly, while intraventricular and His bundle conduction were not altered. The maximal effect of adenosine on the sinus node and AV nodal conduction occurred after 636 +/- 109 and 111 +/- 35 (mean +/- SE) beats, respectively. During programmed stimulation at a cycle length of 250 ms, adenosine reduced atrial ERP in a dose-dependent manner. At cycle lengths of 170 and 200 ms, adenosine increased the atrial ERP at 3 microM, and then progressively shortened the ERP at higher doses. At all adenosine concentrations used, the usual rate-dependent adaption in ERP was suppressed. These observations explain the efficacy of adenosine against supraventricular tachyarrhythmias where the AV-node forms a part of a reentrant circuit. Adenosine shortened the atrial ERP, but at high pacing rates also led to a relative prolongation of the atrial ERP as the rate-dependent adaption was suppressed. These opposite effects of adenosine may explain earlier contradictory findings of its action on atrial arrhythmias.
腺苷的负性变时和变传导作用似乎是其对室上性快速心律失常产生抗心律失常作用的原因。为了进一步明确腺苷对室上性心律失常时心率、传导、不应期的影响，评估了房室结传导减慢和窦性心率降低至稳态的时间。采用高分辨率心电图记录技术，在Langendorff法灌注的离体豚鼠心脏中，测定心率、传导间期和有效不应期的变化。3和10微摩尔浓度的腺苷显著降低窦性心率并延长房室结传导，而室内传导和希氏束传导未改变。腺苷对窦房结和房室结传导的最大作用分别在636±109和111±35（平均值±标准误）次心跳后出现。在250毫秒的周期长度进行程控刺激时，腺苷以剂量依赖的方式降低心房有效不应期。在170和200毫秒的周期长度时，3微摩尔的腺苷增加心房有效不应期，然后在更高剂量时逐渐缩短有效不应期。在所使用的所有腺苷浓度下，有效不应期通常的频率依赖性适应均被抑制。这些观察结果解释了腺苷对室上性快速心律失常的疗效，其中房室结是折返环路的一部分。腺苷缩短心房有效不应期，但在高起搏频率时，由于频率依赖性适应被抑制，也导致心房有效不应期相对延长。腺苷的这些相反作用可能解释了其对房性心律失常作用的早期矛盾发现。
